A mechanistic link between TLE3 loss and glucocorticoid receptor-mediated androgen receptor inhibitor resistance supports the rationale to target GR during anti-hormonal treatment in castrate-resistant prostate cancer.
Prostate cancer resistance to androgen receptor antagonist therapy occurs by way of tumors impeding local glucocorticoid metabolism and inactivation and thereby permitting sustained glucocorticoids to stimulate up-regulated glucocorticoid receptor.
Development of a conditional glucocorticoid receptor knockdown rat model allows for high resolution anatomical, physiological and behavioral exploration into the role of glucocorticoid receptor signaling in defined cell populations.
Stimulation of endothelial glucose metabolism and vascular growth by genetic depletion of endothelial Foxo1 improves the whole-body response to a high-fat diet, by preserving adipose tissue functions and glucose homeostasis.
The high-resolution x-ray structure of an asymmetrical SeCitS dimer, present in the inward- and outward-facing state, provides a complete mechanism of substrate and ion translocation in a sodium-dependent symporter.